Free fatty acids regulate insulin secretion from pancreatic β cells through GPR40

By Y. Itoh, Y. Kawamata, M. Harada, Makoto Kobayashi, Ryo Fujii, S. Fukusumi, K. Ogi, M. Hosoya, Yasuhiro Tanaka, H. Uejima and 12 more. Nature, 2003

1,546 citations recorded by the source corpus.

Subfields: Endocrine and Autonomic Systems, Endocrinology, Diabetes and Metabolism, Surgery

View Paper: https://www.semanticscholar.org/paper/020bf31ace7f8fc5b5d8394a34d49ecc13eb8433

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Endocrine and Autonomic Systems

1. R. Pertwee
2. G. Boden
3. S. Seino
4. F. B. Hu
5. Jerrold M. Olefsky
6. T. Shibasaki
7. V. Di Marzo

In Endocrinology, Diabetes and Metabolism

1. P. Calder
2. F. B. Hu
3. W. Willett
4. Y. Ding
5. Yoshimasa Tanaka
6. E. Gilbert
7. S. Kahn
8. Zhuo Fu

In Surgery

1. Jerrold M. Olefsky
2. F. B. Hu
3. J. Tschopp
4. E. Gilbert
5. S. Kahn
6. S. Seino
7. Zhuo Fu
8. Dongmin Liu

Citations in the corpus

• Risk Factors Contributing to Type 2 Diabetes and Recent Advances in the Treatment and Prevention (2014, background): “The stimulation of GPR40 with FFAs leads to insulin secretion through β-cell-specific signaling pathway, which can be inhibited by the treatment with small interfering RNA [138].”
• Mechanisms linking obesity to insulin resistance and type 2 diabetes (2006, background): “The first relates to the binding of NEFAs to the G-protein-coupled receptor GPR40 on the cell membrane, resulting in the activation of intracellular signalling and a subsequent increase in intracellular calcium and secretory granule exocytosi”
• GPR120 is an omega-3 fatty acid receptor mediating potent anti-inflammatory and insulin-sensitizing effects. (2010, positive): “Recently, several groups reported that five orphan receptors, GPR40, GPR41, GPR43, GPR84, and GPR120, can be activated by free fatty acids (FFAs).”
• Obesity and Free Fatty Acids (FFA) (2008, background): “Third, obesity and FFAs have been shown to induce endoplasmic reticulum stress that can result in activation of IKK, JNK, and inflammatory responses [36], and lastly, several G protein–coupled receptors, including GRP-40 and GRP-120, have been shown to bind FFAs [37,38].”
• Diet, metabolites, and "western-lifestyle" inflammatory diseases. (2014, neutral): “, 2009), GPR40 (Fujita et al., 2011; Itoh et al., 2003),”
• Dietary fats and prevention of type 2 diabetes (2008, background): “While the former, in particular, may mediate effects of FAs on insulin secretion [78,79], GPR41 and GPR43 can be activated by short-chain FFA [80].”
• PKA-dependent and PKA-independent pathways for cAMP-regulated exocytosis. (2005, background): “Olfactory sensory neurons express a variety of GPCRs that activate the G protein G olf , which is similar to the stimulatory G s protein.”
• INFLAMMATION AND LIPID SIGNALING IN THE ETIOLOGY OF INSULIN RESISTANCE (2012, neutral): “There is a family of lipid sensing GPCRs, including GPR40, 41, 43, 84, and 120 (Itoh et al., 2003; Tazoe et al., 2008; Wang et al., 2006), and recent reports have indicated that omega 3 FAs can stimulate GPR120 (Hirasawa et al., 2005; Oh et al., 2010).”